Anistreplase
An acylated inactive complex of streptokinase and human lysine-plasminogen. After injection, the acyl group is slowly hydrolyzed, producing an activator that converts plasminogen to plasmin, thereby initiating fibrinolysis. Its half-life is about 90 minutes compared to 5 minutes for TPA; (TISSUE PLASMINOGEN ACTIVATOR); 16 minutes for UROKINASE-TYPE PLASMINOGEN ACTIVATOR and 23 minutes for STREPTOKINASE. If treatment is initiated within 3 hours of onset of symptoms for acute myocardial infarction, the drug preserves myocardial tissue and left ventricular function and increases coronary artery patency. Bleeding complications are similar to other thrombolytic agents.
Thrombolytic Therapy
Streptokinase
Controlled Clinical Trials as Topic
Works about clinical trials involving one or more test treatments, at least one control treatment, specified outcome measures for evaluating the studied intervention, and a bias-free method for assigning patients to the test treatment. The treatment may be drugs, devices, or procedures studied for diagnostic, therapeutic, or prophylactic effectiveness. Control measures include placebos, active medicines, no-treatment, dosage forms and regimens, historical comparisons, etc. When randomization using mathematical techniques, such as the use of a random numbers table, is employed to assign patients to test or control treatments, the trials are characterized as RANDOMIZED CONTROLLED TRIALS AS TOPIC.
Myocardial Infarction
Penicillin V
Encyclopedias as Topic
Penicillins
A group of antibiotics that contain 6-aminopenicillanic acid with a side chain attached to the 6-amino group. The penicillin nucleus is the chief structural requirement for biological activity. The side-chain structure determines many of the antibacterial and pharmacological characteristics. (Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1065)
Penicillin G
A penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It has also been used as an experimental convulsant because of its actions on GAMMA-AMINOBUTYRIC ACID mediated synaptic transmission.
Ampicillin
Penicillin Amidase
Carbenicillin
Journal Impact Factor
Pharmacology
Pharmacology, Clinical
Publishing
Bibliometrics
Journalism, Medical
Tissue Plasminogen Activator
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.
Emergency Medical Services
Antithrombin Proteins
An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance.
Antithrombins
beta-Alanine
An amino acid formed in vivo by the degradation of dihydrouracil and carnosine. Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, the compound may be a false transmitter replacing GAMMA-AMINOBUTYRIC ACID. A rare genetic disorder, hyper-beta-alaninemia, has been reported.
Hirudins
Single-chain polypeptides of about 65 amino acids (7 kDa) from LEECHES that have a neutral hydrophobic N terminus, an acidic hydrophilic C terminus, and a compact, hydrophobic core region. Recombinant hirudins lack tyr-63 sulfation and are referred to as 'desulfato-hirudins'. They form a stable non-covalent complex with ALPHA-THROMBIN, thereby abolishing its ability to cleave FIBRINOGEN.
Drug Eruptions
Tooth Eruption
Lichenoid Eruptions
Conditions in which there is histological damage to the lower epidermis along with a grouped chronic inflammatory infiltrate in the papillary dermis disturbing the interface between the epidermis and dermis. LICHEN PLANUS is the prototype of all lichenoid eruptions. (From Rook et al., Textbook of Dermatology, 4th ed, p398)
Aspirin
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
Heparin
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
Plasminogen
Magnetite Nanoparticles
Nanoparticles
Magnetic Resonance Spectroscopy
Sensitivity and Specificity
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
Risk Factors
Ventricular Dysfunction, Left
A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.
Coronary Disease
Thrombolytic therapy in Europe: current status. (1/39)
Thrombolytic therapy is a practical, effective approach to the management of acute myocardial infarction that is widely used in Europe today. Early European trials demonstrated a clear reduction in mortality in patients who received thrombolytic therapy compared with those given conventional treatment. The findings of experimental studies suggest that early reperfusion of the infarct-related artery reduces myocardial damage, which results in the preservation of left ventricular function and, in turn, may improve survival. Although tissue plasminogen activator (t-PA) has been shown to produce more rapid and complete reperfusion than streptokinase, two large-scale clinical trials in which t-PA was given as a standard 3- or 4-h infusion provided no evidence of a survival advantage with this agent. However, the accelerated t-PA regimen used in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) study was associated with a lower mortality than streptokinase or a combination of t-PA and streptokinase, thus lending support to the 'open artery' theory. Two recent studies conducted in Europe, the Grampian Region Early Anistreplase Trial (GREAT) and the European Myocardial Infarction Project (EMIP), have demonstrated the feasibility, safety, and efficacy of early thrombolytic therapy before admission to hospital. In GREAT, anistreplase (APSAC) was administered at home by general practitioners. In EMIP, this same agent was given by emergency medical personnel. In both studies, pre-hospital administration reduced the time between the onset of symptoms and initiation of thrombolysis and was associated with a lower mortality rate. Recent data from the European Cooperative Group Study show that the benefits of thrombolytic therapy are maintained for up to 5 years. Research continues in an effort to develop safer and more effective thrombolytic agents. Educational efforts to familiarize the public with the symptoms of myocardial infarction and the development of more rapid, efficient emergency response systems may also improve the outcome of thrombolytic therapy by shortening the time between symptom onset and thrombolytic drug administration. (+info)Monitoring of streptokinase resistance titre in acute myocardial infarction patients up to 30 months after giving streptokinase or anistreplase and related studies to measure specific antistreptokinase IgG. (2/39)
OBJECTIVE: To examine the induction of antistreptokinase antibodies after giving streptokinase or anistreplase to patients with acute myocardial infarction. DESIGN: Patients were randomly allocated to receive either 1.5 x 10(6) IU, streptokinase or 30U anistreplase in a double blind study. Blood samples were collected immediately before treatment and subsequently at intervals up to 30 months; plasma samples were assayed for streptokinase resistance titre (functional assay) and streptokinase binding by IgG (microradioimmunoassay). SETTING: Cardiology department in a general hospital. PATIENTS: 128 consecutive eligible patients. Samples were collected for up to one year according to a prospective design: a subsection of 47 patients was selected for intensive study over the first 14 days. After one year, all available patients (67) were sampled on one further occasion. RESULTS: Antibody responses to streptokinase and anistreplase were similar. Streptokinase resistance titres exceeded pretreatment concentrations five days after dosing, and values peaked at 14 days. By 12 months after dosing, 92% of resistance titres (n = 84) had returned to within the pretreatment range. Antistreptokinase IgG concentrations also exceeded baseline concentrations within five days and peaked at 14 days. Half of the individual values had returned to within the pretreatment range by 12 months (n = 84) and 89% by 30 months (n = 18). CONCLUSION: Although we cannot be sure of the clinical significance, because of the increased likelihood of resistance due to antistreptokinase antibody, streptokinase and anistreplase may not be effective if administered more than five days after an earlier dose of streptokinase or anistreplase, particularly between five days and 12 months, and increased antistreptokinase antibody may increase the risk of allergic-type reactions. (+info)Feasibility, safety, and efficacy of domiciliary thrombolysis by general practitioners: Grampian region early anistreplase trial. GREAT Group. (3/39)
OBJECTIVE: To assess the feasibility, safety, and efficacy of domiciliary thrombolysis by general practitioners. DESIGN: Randomised double blind parallel group trial of anistreplase 30 units intravenously and placebo given either at home or in hospital. SETTING: 29 rural practices in Grampian admitting patients to teaching hospitals in Aberdeen (average distance 36 (range 16-62) miles). PATIENTS: 311 patients with suspected acute myocardial infarction and no contraindications to thrombolytic therapy seen at home within four hours of onset of symptoms. MAIN OUTCOME MEASURES: Time saving, adverse events, Q wave infarction, left ventricular function. RESULTS: Anistreplase was administered at home 101 minutes after onset of symptoms, while anistreplase was given in hospital 240 minutes after onset of symptoms (median times). Adverse events after thrombolysis were infrequent and, apart from cardiac arrest, not a serious problem when they occurred in the community: seven of 13 patients were resuscitated after cardiac arrest out of hospital. By three months after trial entry the relative reduction of deaths from all causes in patients given thrombolytic therapy at home was 49% (13/163 (8.0%) v 23/148 (15.5%); difference -7.6% (95% confidence interval -14.7% to -0.4%), p = 0.04). Full thickness Q wave infarction was less common in patients with confirmed infarction receiving treatment at home (65/122 (53.3%) v 76/112 (67.9%); difference -14.6% (95% confidence interval -27.0% to -2.2%), p = 0.02). CONCLUSIONS: General practitioners provided rapid pre-hospital coronary care of a high standard. Compared with later administration in hospital, giving anistreplase at home resulted in reduction in mortality, fewer cardiac arrests, fewer Q wave infarcts, and better left ventricular function. Benefits were most marked where thrombolytic therapy was administered within two hours of the onset of symptoms. (+info)Oesophageal dissection after thrombolytic treatment for myocardial infarction. (4/39)
A 62 year old woman admitted with a history suggesting acute myocardial infarction had thrombolytic treatment with anisoylated plasminogen-streptokinase activator complex, which resulted in submucosal haemorrhage in the oesophagus; this caused dissection of the wall of the oesophagus and complete dysphagia. The haematoma resolved spontaneously, leaving behind a diverticulum, with reduced peristalsis and delayed emptying but no obstruction. (+info)The pharmacological modulation of thrombin-induced cerebral thromboembolism in the rabbit. (5/39)
1. Intracarotid (i.c.) administration of thrombin induced a marked accumulation of 111indium-labelled platelets and 125I-labelled fibrinogen within the cranial vasculature of anaesthetized rabbits. 2. Thrombin (100 iu kg-1, i.c.) - induced platelet accumulation was completely abolished by pretreatment with desulphatohirudin (CGP 39393; 1 mg kg-1 i.c., 1 min prior to thrombin). Administration of CGP 39393 1 or 20 min after thrombin produced a significant reduction in platelet accumulation. 3. Intravenous (i.v.) administration of the platelet activating factor (PAF) receptor antagonist BN 52021 (10 mg kg-1) 5 min prior to thrombin (100 iu kg-1, i.c.) had no effect on platelet accumulation. 4. An inhibitor of NO biosynthesis, L-NG-nitro arginine methyl ester (L-NAME; 100 mg kg-1, i.c.), had no significant effect on the cranial platelet accumulation response to thrombin (10 iu kg-1, i.c.) when administered 5 min prior to thrombin. 5. Defibrotide (32 or 64 mg kg-1 bolus i.c. followed by 32 or 64 mg kg-1 h-1, i.c., infusion for 45 min) treatment begun 20 min after thrombin (100 iu kg-1, i.c.) did not significantly modify the cranial platelet accumulation response. 6. Cranial platelet accumulation induced by thrombin (100 iu kg-1, i.c.) was significantly reversed by the fibrinolytic drugs urokinase (20 iu kg-1, i.c., infusion for 45 min), anisoylated plasminogen streptokinase activator complex (APSAC) (200 micrograms kg-1, i.v. bolus) or recombinant tissue plasminogen activator (rt-PA; 100 micrograms kg-1, i.c. bolus followed by 20 micrograms kg-1 min-1, i.c., infusion for 45 min) administered 20 min after thrombin.8. These results suggest that neither endogenous PAF nor NO modulate thrombin-induced intracranial platelet accumulation in the rabbit. However, fibrin deposition appears to play an important role as shown by the ability of fibrinolytic agents to reverse platelet and fibrinogen accumulation induced by i.c. thrombin. (+info)Clinical and economic outcomes in thrombolytic treatment of peripheral arterial occlusive disease and deep venous thrombosis. (6/39)
PURPOSE: Over the past 2 decades the use of thrombolytic therapy in the management of peripheral occlusive diseases, most notably peripheral arterial occlusion (PAO) and deep venous thrombosis (DVT), has become an accepted and potentially preferable alternative to surgery. We examined the period when urokinase was in short supply and subsequently unavailable, to explore potential differences in clinical outcome and economic effect between urokinase and recombinant tissue plasminogen activator (rt-PA). MATERIAL AND METHODS: Data were obtained from the Premier Perspective Database, a broad clinical database that contains information on inpatient medical practices and resource use. The study population included all patients hospitalized in 1999 and 2000 with a primary or secondary diagnosis of PAO or DVT. Incidence was calculated for common adverse events, including bleeding complications, intracranial hemorrhage, amputation, and death. Cost data were also abstracted from the database, and are expressed as mean +/- SD. RESULTS: Demographic variables were similar in the urokinase and rt-PA groups. The rate of bleeding complications was similar in the urokinase and rt-PA groups. There were no intracranial hemorrhages in the urokinase group, compared with a rate of 1.5% in the rt-PA PAO group (P = .087) and 1.9% in the rt-PA DVT group (P = .175). The in-hospital mortality rate was lower in the urokinase-treated PAO subgroup (3.6% vs 8.5%; P = .026), but a similar finding in the DVT subgroup did not achieve statistical significance (4% vs 9.8%; P = .069). While pharmacy costs were greater in the urokinase-treated group (US 5472 dollars +/- US 5579 dollars vs US 3644 dollars +/- US 6009 dollars, P < .001; PAO subgroup, US 11,070 dollars +/- US 15,409 dollars vs US 6150 dollars +/- US 12,398 dollars, P = .003), overall hospital costs did not differ significantly between the 2 groups. This finding appears to be explained by a shorter hospital stay and reduced room and board costs in the urokinase-treated group. CONCLUSION: There were significant differences in outcome in patients with PAO and DVT who received treatment with urokinase and rt-PA. While pharmacy costs were significantly greater when urokinase was used, reduction in length of stay accounted for similar total hospital costs compared with rt-PA. These findings must be considered in the context of the retrospective nature of the analysis and the potential to use dosing regimens that differ from those in this study. (+info)Serum myoglobin and creatine kinase enzymes in acute myocardial infarction treated with Anistreplase. (7/39)
AIMS: To compare plasma myoglobin concentration and cardiac enzyme activity with electrocardiographic (ECG) changes in two groups of patients (reperfused and non-reperfused) participating in a placebo-controlled randomised double blind trial of treatment of myocardial infarction (MI) with intravenous thrombolytic therapy (Anistreplase). METHODS: Twenty two patients with confirmed MI obeying strict inclusion and exclusion criteria were studied. Plasma myoglobin was measured by radioimmunoassay and creatine kinase enzyme (CK and CKMB) by NAC activated and NAC activated/immunoinhibition methods respectively in all patients before and at frequent intervals after injection of Anistreplase or placebo. Patients were divided into reperfused (R) and non-reperfused (NR) groups on the basis of ECG criteria. Reperfusion was diagnosed if the measured ST segment elevation fell by greater than or equal to 50% at 2 hours post dosing. RESULTS: The time to peak (TTP) myoglobin was significantly less in the R group compared with the NR group but there was considerable overlap in the range of values. The area under the enzyme time curves (AUCs) and summed ST segment epsilon ST elevations were significantly smaller in the R compared with the NR group. CONCLUSIONS: Although TTP myoglobin results were significantly lower in the R group, TTP myoglobin will probably not be useful as an non-invasive indicator of reperfusion because of the overlap in values between the two groups. The significant reduction in the AUC and epsilon ST only in the R group suggests decreased infarct size. However, in this small preliminary study reperfusion did not occur more frequently with Anistreplase than without. (+info)Evaluation of thrombolytic and systemic effects of the novel recombinant plasminogen activator BM 06.022 compared with alteplase, anistreplase, streptokinase and urokinase in a canine model of coronary artery thrombosis. (8/39)
The thrombolytic and systemic effects of BM 06.022 were evaluated and compared with those of alteplase, anistreplase, streptokinase and urokinase in a canine model of coronary artery thrombosis. BM 06.022 consists of the kringle-2 and protease domains of human tissue plasminogen activator (t-PA) and is unglycosylated because of its expression in Escherichia coli cells. Thrombus formation in anesthetized open chest dogs was induced by electrical injury to the intimal surface of the left circumflex coronary artery at a high level site of obstruction. In heparinized dogs, none of six vehicle-treated animals exhibited reperfusion. Reperfusion was achieved in four of six dogs at 18.3 +/- 6 min after intravenous bolus injection of 140 kU/kg (0.24 mg/kg) of BM 06.022, whereas four of six dogs exhibited reperfusion later (p less than 0.05) at 76.5 +/- 16.1 min during infusion of 1.33 mg/kg of alteplase (0.13 mg/kg as initial bolus injection, followed by 0.66 mg/kg over 1 h and 0.53 mg/kg over 2 h). Significantly later (p less than 0.05) reperfusion than that achieved with BM 06.022 was achieved in five of six dogs at 57.8 +/- 12.1 min after intravenous injection of 0.4 U/kg of anistreplase. Streptokinase (21,000 IU/kg over 60 min) and urokinase (20,000 IU/kg as an intravenous bolus injection, followed by 20,000 IU/kg over 89 min) each induced reperfusion in three of six dogs but at 67 +/- 12 and 84.3 +/- 17.1 min (p less than 0.05 vs. BM 06.022), respectively.(ABSTRACT TRUNCATED AT 250 WORDS) (+info)
Drug eruptions and isotypic antibody responses to streptokinase after infusions of anisoylated plasminogen-streptokinase...
ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs...
Does thrombolysis in myocardial infarction (TIMI) perfusion grade 2 represent a mostly patent artery or a mostly occluded...
WHOCC - ATC/DDD Index
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Beecham Group
Eminase (anistreplase). *Engerix-B (hepatitis B vaccine). *Floxapen (flucloxacillin). *granisetron. *Havrix (hepatitis A ...
ATC code B01
B01AD03 Anistreplase. B01AD04 Urokinase. B01AD05 Fibrinolysin. B01AD06 Brinase. B01AD07 Reteplase. B01AD08 Saruplase. B01AD09 ...
Fibrinolysis
Anistreplase Desmoteplase Streptokinase Nattokinase Lumbrokinase Serrapeptase Papain DNase Bromelain Honokiol Dugdale, David et ...
APSAC
... anistreplase) This disambiguation page lists articles associated with the title APSAC. If an internal link led you here, you ...
List of MeSH codes (D12.776.124)
... anistreplase MeSH D12.776.124.125.662.537.900 - streptodornase and streptokinase MeSH D12.776.124.125.662.768 - tissue ...
List of drugs: An-Ap
... anistreplase (INN) anitrazafen (INN) anivamersen (USAN, INN) Anodynos-DHC Anolor 300 Anoquan anpirtoline (INN) anrukinzumab ( ...
List of MeSH codes (D08)
... anistreplase MeSH D08.811.277.656.300.775.900 - streptodornase and streptokinase MeSH D08.811.277.656.350 - exopeptidases MeSH ... anistreplase MeSH D08.811.277.656.300.760.640 - proprotein convertase 1 MeSH D08.811.277.656.300.760.646 - proprotein ...
Thrombolysis
Anistreplase (Eminase) Recombinant tissue plasminogen activators (rtPA) Alteplase (Activase or Actilyse) Reteplase (Retavase) ...
International Studies of Infarct Survival
... and anistreplase to each other, and also compared the anticoagulant heparin to no heparin. All patients were also given aspirin ... a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin ...
Anistreplase
... is a thrombolytic drug. It is also known as anisoylated plasminogen streptokinase activator complex (APSAC) after ... Anistreplase has been developed by Beecham as Eminase. It is also known as anisoylated plasminogen streptokinase activator ... Grampion Region Early Anistreplase Trial (GREAT)". J Epidemiol Community Health. 47 (5): 377-381. doi:10.1136/jech.47.5.377. ... "Assessment of the practicality and safety of thrombolysis with anistreplase given by general practitioners". Br J Gen Pract. 45 ...
Drotrecogin alfa
In 2001, Eli Lilly's chairman, president and CEO, Sidney Taurel, told shareholders: "No medicine better symbolizes our mission than Xigris," calling it "one of our industry's genuine breakthroughs."[5]. Xigris was designed to fight sepsis, a condition that kills more than 200,000 Americans annually. It was the only approved drug for sepsis, and it costs $8,000 to treat a single patient. Lilly hoped it would be a blockbuster, with sales of at least a billion dollars a year. But after five years on the market, sales were only $200 million.. Eli Lilly used the Belsito & Company PR firm in a marketing campaign to promote Xigris, its drug for treatment of sepsis. A report in the New England Journal of Medicine (NEJM) accused the company of initiating false reports of a shortage of the drug to boost sales.[6] Belsito and Company spread the word that the drug was being "rationed" and physicians were being 'systematically forced' to decide who would live and who would die. As part of this effort, Lilly ...
Aspirin
Acetylsalicylic acid is a weak acid, and very little of it is ionized in the stomach after oral administration. Acetylsalicylic acid is quickly absorbed through the cell membrane in the acidic conditions of the stomach. The increased pH and larger surface area of the small intestine causes aspirin to be absorbed more slowly there, as more of it is ionised. Owing to the formation of concretions, aspirin is absorbed much more slowly during overdose, and plasma concentrations can continue to rise for up to 24 hours after ingestion.[152][153][154] About 50-80% of salicylate in the blood is bound to albumin protein, while the rest remains in the active, ionized state; protein binding is concentration-dependent. Saturation of binding sites leads to more free salicylate and increased toxicity. The volume of distribution is 0.1-0.2 L/kg. Acidosis increases the volume of distribution because of enhancement of tissue penetration of salicylates.[154] As much as 80% of therapeutic doses of salicylic acid is ...
Vitamin K antagonist
These drugs deplete the active form of the vitamin by inhibiting the enzyme vitamin K epoxide reductase and thus the recycling of the inactive vitamin K epoxide back to the active reduced form of vitamin K. The drugs are structurally similar to vitamin K and act as competitive inhibitors of the enzyme. The term "vitamin K antagonist" is a misnomer, as the drugs do not directly antagonise the action of vitamin K in the pharmacological sense, but rather the recycling of vitamin K. Vitamin K is required for the proper production of certain proteins involved in the blood clotting process. For example, it is needed to carboxylate specific glutamic acid residues on prothrombin. Without these residues carboxylated, the protein will not form the appropriate conformation of thrombin, which is needed to produce the fibrin monomers that are polymerized to form clots.[1] The action of this class of anticoagulants may be reversed by administering vitamin K for the duration of the anticoagulant's residence in ...
Prostacyclin
The drug is clear with a pH of 10.[7] Its production is inhibited indirectly by NSAIDs, which inhibit the cyclooxygenase enzymes COX1 and COX2. These convert arachidonic acid to prostaglandin H2 (PGH2), the immediate precursor of prostacyclin. Since thromboxane (an eicosanoid stimulator of platelet aggregation) is also downstream of COX enzymes, one might think that the effect of NSAIDs would act to balance. However, prostacyclin concentrations recover much faster than thromboxane levels, so aspirin administration initially has little to no effect but eventually prevents platelet aggregation (the effect of prostaglandins predominates as they are regenerated). This is explained by understanding the cells that produce each molecule, TXA2 and PGI2. Since PGI2 is primarily produced in a nucleated endothelial cell, the COX inhibition by NSAID can be overcome with time by increased COX gene activation and subsequent production of more COX enzymes to catalyze the formation of PGI2. In contrast, TXA2 is ...
Sibrafiban
... (Ro 48-3657, proposed brand name Xubix) is the double prodrug of Ro-44-3888, which is a platelet aggregation inhibitor. It was being developed for secondary prevention of arterial thrombosis following unstable angina pectoris and acute myocardial infarction (MI). On August 6, 1999, Hoffmann-La Roche announced that the preliminary results from Phase III clinical trials had not shown that sibrafiban was better than aspirin in preventing recurrent ischemic events in patients suffering from acute coronary syndrome. The development of sibrafiban was terminated. ...
Ethylenediaminetetraacetic acid
In industry, EDTA is mainly used to sequester metal ions in aqueous solution. In the textile industry, it prevents metal ion impurities from modifying colors of dyed products. In the pulp and paper industry, EDTA inhibits the ability of metal ions, especially Mn2+, from catalyzing the disproportionation of hydrogen peroxide, which is used in chlorine-free bleaching. In a similar manner, EDTA is added to some food as a preservative or stabilizer to prevent catalytic oxidative decoloration, which is catalyzed by metal ions.[4] In soft drinks containing ascorbic acid and sodium benzoate, EDTA mitigates formation of benzene (a carcinogen).[5] The reduction of water hardness in laundry applications and the dissolution of scale in boilers both rely on EDTA and related complexants to bind Ca2+, Mg2+, as well as other metal ions. Once bound to EDTA, these metal centers tend not to form precipitates or to interfere with the action of the soaps and detergents. For similar reasons, cleaning solutions often ...
Clopidogrel
As of March 2017, brands included Aclop, Actaclo, Agregex, Agrelan, Agrelax, Agreless, Agrelex, Agreplat, Anclog, Angiclod, Anplat, Antiagrex, Antiban, Antigrel, Antiplaq, Antiplar, Aplate, Apolets, Areplex, Artepid, Asogrel, Atelit, Atelit, Ateplax, Atervix, Atheros, Athorel, Atrombin, Attera, Bidogrel, Bigrel, Borgavix, Carder, Cardogrel, Carpigrel, Ceraenade, Ceruvin, Cidorix, Clatex, Clavix, Clentel, Clentel, Clidorel, Clodel, Clodelib, Clodian, Clodil, Cloflow, Clofre, Clogan, Clogin, Clognil, Clogrel, Clogrelhexal, Clolyse, Clont, Clood, Clopacin, Clopcare, Clopeno, Clopex Agrel, Clopez, Clopi, Clopid, Clopida, Clopidep, Clopidexcel, Clopidix, Clopidogrel, Clopidogrelum, Clopidomed, Clopidorex, Clopidosyn, Clopidoteg, Clopidowel, Clopidra, Clopidrax, Clopidrol, Clopigal, Clopigamma, Clopigrel, Clopilet, Clopimed, Clopimef, Clopimet, Clopinovo, Clopione, Clopiright, Clopirite, Clopirod, Clopisan, Clopistad, Clopistad, Clopitab, Clopithan, Clopitro, ClopiVale, Clopivas, Clopivaz, Clopivid, ...
Miokardio infartu akutu, entziklopedia askea.
Anistreplase (en) , pharmaceutical preparation of nitroglycerin (en) , carvedilol (en) , verapamil (en) , carvedilol (en) eta ...
阿司匹林 - 維基百科,自由的百科全書
Anistreplase) · 孟替普酶(英語:Monteplase) 其他絲氨酸內肽酶: 安克洛酶(英語:Ancrod) · 纖維蛋白酶(英語:Brinase
肝素 - 维基百科,自由的百科全书
Anistreplase) · 孟替普酶(英语:Monteplase) 其他丝氨酸内肽酶: 安克洛酶(英语:Ancrod) · 纤维蛋白酶(英语:Brinase
Anistreplase - Wikipedia
Anistreplase is a thrombolytic drug. It is also known as anisoylated plasminogen streptokinase activator complex (APSAC) after ... Anistreplase has been developed by Beecham as Eminase. It is also known as anisoylated plasminogen streptokinase activator ... Grampion Region Early Anistreplase Trial (GREAT)". J Epidemiol Community Health. 47 (5): 377-381. doi:10.1136/jech.47.5.377. ... "Assessment of the practicality and safety of thrombolysis with anistreplase given by general practitioners". Br J Gen Pract. 45 ...
ANISTREPLASE - INJECTION (Eminase) side effects, medical uses, and drug interactions.
Anistreplase - DrugBank
Eminase is a lyophilized (freeze-dried) formulation of anistreplase, the p-anisoyl derivative of the primary Lys-plasminogen- ... Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. This in turn leads to the degradation of blood clots. ... Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the ... Anistreplase. Accession Number. DB00029 (BTD00102, BIOD00102) Type. Biotech. Groups. Approved. Biologic Classification. Protein ...
Anistreplase - A-Z Drugs - Benefits of
Anistreplase is a drug used to stop blood clots. Analysis has proven that this drug is efficient in decreasing the chance of ... Whats Anistreplase for?. Anistreplase is a drug used to stop blood clots. Analysis has proven that this drug is efficient in ... 4.1 What should be identified earlier than utilizing Anistreplase? 4.2 Is Anistreplase protected for pregnant or breastfeeding ... In what dosages and preparations is Anistreplase obtainable?. Anistreplase obtainable within the following dosages: ...
Anistreplase: Uses, Interactions, Mechanism of Action | DrugBank Online
Anistreplase is a form of recombinant human tissue plasminogen activator used in the emergency treatment of myocardial ... Anistreplase. Identification. Summary. Anistreplase is a form of recombinant human tissue plasminogen activator used in the ... Anistreplase. Clinical Trials. Clinical Trials Phase. Status. Purpose. Conditions. Count. Pharmacoeconomics. Manufacturers. Not ... Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. This in turn leads to the degradation of blood clots. ...
Anistreplase (anisoylated plasminogen-streptokinase activator complex, APSAC) | Davis's Drug Guide
Find information on Anistreplase (anisoylated plasminogen-streptokinase activator complex, APSAC) in Daviss Drug Guide ... anistreplase is a topic covered in the Daviss Drug Guide. To view the entire topic, please sign in or purchase a subscription. ... "Anistreplase." Daviss Drug Guide, 16th ed., F.A. Davis Company, 2020. Nursing Central, nursing.unboundmedicine.com/ ... nursingcentral/view/Davis-Drug-Guide/109358/all/anistreplase. Quiring C, Sanoski CA, Vallerand AH. Anistreplase. Daviss Drug ...
Anisoylated plasminogen streptokinase activator complex | definition of anisoylated plasminogen streptokinase activator complex...
anistreplase. (redirected from anisoylated plasminogen streptokinase activator complex). Also found in: Acronyms. anistreplase ... anistreplase. See APSAC. anistreplase. A clot-dissolving drug used to try to re-establish blood flow in the heart muscle in the ... anistreplase. /an·is·trep·lase/ (an″is-trep´lās) a thrombolytic agent used to clear coronary vessel occlusions associated with ... anistreplase. a plasminogen activator. indication This drug is used in acute MI for lysis of coronary artery thrombi. ...
Beecham Group - Wikipedia
ATC code B01 - Wikipedia
April 1995 - Volume 25 - Issue 4 : Journal of Cardiovascular Pharmacology
Coronary Artery Disease - RxMed.com
Dabigatran Advanced Patient Information - Drugs.com
Dalteparin (Subcutaneous Route) Proper Use - Mayo Clinic
This medicine may increase your chance of bleeding or bruising. This risk is higher if you have poorly controlled high blood pressure, a heart infection, ulcers of the stomach, or other bleeding problems. Check with your doctor right away if you notice any unusual bleeding or bruising, black, tarry stools, blood. in the urine or stools, or pinpoint red spots on your skin. Avoid picking your nose. If you need to blow your nose, blow it gently. This medicine may increase your chance of serious bleeding or nerve problems in your spine. This risk is higher if you have a catheter in your back for pain medicine or anesthetics, or have an injection into your spine (sometimes called an "epidural" or "spinal"). Other things that increase this risk are traumatic or repeated epidural or spinal punctures in the past, spinal deformity, previous spinal surgery, or use of other medications that increase the risk of bleeding. Check with your doctor right away if you develop weakness or numbness in your legs or ...
Pentosan Polysulfate Sodium (Oral Route) Precautions - Mayo Clinic
Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.. Using this medicine with any of the following medicines is usually not recommended, but may be required in some cases. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines.. ...
Prehospital thrombolytic therapy in patients with suspected acute myocardial infarction
Dabigatran Etexilate Mesylate
Drug eruptions and isotypic antibody responses to streptokinase after infusions of anisoylated plasminogen-streptokinase...
N2 - Background: Anisoylated plasminogen-streptokinase complex (APSAC, anistreplase) is a thrombolytic agent (131 kd) used for ... AB - Background: Anisoylated plasminogen-streptokinase complex (APSAC, anistreplase) is a thrombolytic agent (131 kd) used for ... Background: Anisoylated plasminogen-streptokinase complex (APSAC, anistreplase) is a thrombolytic agent (131 kd) used for ... abstract = "Background: Anisoylated plasminogen-streptokinase complex (APSAC, anistreplase) is a thrombolytic agent (131 kd) ...
ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs...
A randomized trial of intravenous heparin in conjunction with anistreplase (anisoylated plasminogen streptokinase activator...
A randomized trial of intravenous heparin in conjunction with anistreplase (anisoylated plasminogen streptokinase activator ... OBJECTIVES: We designed a randomized trial to evaluate the effects of heparin administration in conjunction with anistreplase ( ... A randomized trial of intravenous heparin in conjunction with anistreplase (anisoylated plasminogen streptokinase activator ...
Patent US20060201601 - Flexible markers - Google Patents
Plasminogen activator, tissue type regulates germinal vesicle breakdown and cumulus expansion of bovine cumulus-oocyte complex...
Safety and Effectiveness of tPA in Intra-Abdominal Abscesses
Fibrin Modulating Agents - DrugBank
MEDLINE - Resultado p gina 1
Anistreplase/administra o & dosagem. Anistreplase/farmacocin tica. Anistreplase/uso terap utico. Doen as Cardiovasculares/ ... Anistreplase/economia. Anistreplase/uso terap utico. Institutos de Cardiologia. Estudos de Coortes. Servi os de Sa de Comunit ... Anistreplase/uso terap utico. Servi os M dicos de Emerg ncia/estat stica & dados num ricos. Fibrinol ticos/uso terap utico. ... Anistreplase/uso terap utico. Feminino. Seres Humanos. Masculino. Meia-Idade. Infarto do Mioc rdio/mortalidade. Pa ses Baixos. ...
Peripheral Thrombolysis Imaging: Overview, Choice of Agent and Mechanism of Action, Acute and Chronic Ischemia
Patente US8102176 - NMR device for detection of analytes - Google Patentes
... anistreplase, streptokinase and urokinase; hormones and hormone modifiers, such as bromocriptine; abortifacients, such as ... anistreplase, streptokinase, and urokinase; dermatological agents, such as colchicine, isotretinoin, methotrexate, minoxidil, ... anistreplase, brinase, drotrecogin alfa, fibrinolysin, procein C, reteplase, saruplase, streptokinase, tenecteplase, and ... anistreplase, streptokinase and urokinase; antiemetics, such as prochlorperazine; salicylate gastrointestinal anti-inflammatory ...
Similar Drugs Flashcards by Suzie Ilagan | Brainscape
NREMT Paramedic Medications by Ricky Olivarez
Heart failure post-myocardial infarction: a review of the issues | Heart
Anistreplase, the thrombolytic agent used in GREAT, could be given as a single injection, which enabled domiciliary use. ... Halving of mortality at 1 year by domiciliary thrombolysis in the Grampian Region early anistreplase trial (GREAT). J Am Coll ... who were seen by their general practitioner within four hours of symptom onset and were given intravenous anistreplase either ...
Alteplase5
- Accelerated alteplase vs. anistreplase for angiographic patency in acute MI. (acc.org)
- Thrombolytic therapy uses drugs called thrombolytic agents, such as alteplase (Activase), anistreplase (Eminase), streptokinase (Streptase, Kabikinase), urokinase (Abbokinase), and tissue plasminogen activator (TPA) to dissolve clots. (encyclopedia.com)
- Heparin has an established role as an adjunctive agent in patients receiving alteplase, reteplase, or tenecteplase but should not be used with nonselective fibrinolytic agents such as streptokinase and anistreplase. (slideshare.net)
- The DDDs of streptokinase, alteplase, anistreplase and reteplase are based on thrombolytic treatment in connection with acute myocardial infarction. (whocc.no)
- OR (anistreplase or streptodornase or streptokinase or urokinase or pro?urokinase or rpro?uk or lumbrokinase or duteplase or lanoteplase or pamiteplase or reteplase or saruplase or staphylokinase or streptase or alteplase).ti. (bestbets.org)
APSAC4
- Background: Anisoylated plasminogen-streptokinase complex (APSAC, anistreplase) is a thrombolytic agent (131 kd) used for treatment of myocardial infarction. (northwestern.edu)
- OBJECTIVES: We designed a randomized trial to evaluate the effects of heparin administration in conjunction with anistreplase (anisoylated plasminogen streptokinase activator complex [APSAC]) on arterial patency and clinical end points. (duke.edu)
- Anistreplase (anisoylated plasminogen streptokinase activator complex, or APSAC) was the first custom-designed biochemically modified fibrinolytic agent to be developed (67,68). (78stepshealth.us)
- To evaluate their true functional significance, perfusion grades were compared with enzymatic and electrocardiographic (ECG) indexes of myocardial infarction in 359 patients treated within 4 h with anistreplase (APSAC) or streptokinase. (onlinejacc.org)
Streptokinase activator complex2
- Eminase is a lyophilized (freeze-dried) formulation of anistreplase, the p-anisoyl derivative of the primary Lys-plasminogen-streptokinase activator complex (a complex of Lys-plasminogen and streptokinase). (drugbank.ca)
- A randomized trial of intravenous heparin in conjunction with anistreplase (anisoylated plasminogen streptokinase activator complex) in acute myocardial infarction: the Duke University Clinical Cardiology Study (DUCCS) 1. (duke.edu)
Myocardial infarction2
- Anistreplase is a form of recombinant human tissue plasminogen activator used in the emergency treatment of myocardial infarction and pulmonary emboli. (drugbank.com)
- Cannon CP, McCabe CH, Diver DJ, Herson S, Greene RM, Shah PK, et al: Loaded recombinant tissue-type plasminogen activator, anistreplase and combination thrombolytic therapy for acute myocardial infarction (TIMI) 4 trial. (medigraphic.com)
Plasminogen activator1
- Serial blood samples were obtained before and at 90 min and 24 and 48 h after the administration of streptokinase (15 patients), recombinant tissue-type plasminogen activator (15 patients) or anistreplase (13 patients). (elsevier.com)
Early anistreplase2
- Feasibility, safety, and efficacy of domiciliary thrombolysis by general practitioners: Grampian region early anistreplase trial. (springer.com)
- One study, the Grampian Region Early Anistreplase Trial (GREAT), demonstrated a statistically significant mortality difference in rural patients receiving prehospital thrombolysis, 8 but no urban study to date has been sufficiently powered to demonstrate a similar mortality benefit. (bmj.com)
Eminase2
- Anistreplase has been developed by Beecham as Eminase. (wikipedia.org)
- 2) Aspirin/Anticoagulant Following Thrombolysis with anistreplase (Eminase) in Recurrent Infarction. (thefreedictionary.com)
Aspirin1
- A trial comparing major acute cardiac events (MACE) rates in patients managed with aspirin or anticoagulation (anistreplase) post-thrombolysis for acute MI. (thefreedictionary.com)
Thrombolysis2
- 1) Anistreplase Following Thrombolysis Effect on Reocclusion. (thefreedictionary.com)
- Fibrinolyse en trombolyse [Fribrinolysis and thrombolysis]. (springer.com)
Interactions1
- This intensive review analyzes the effectiveness and drug displacement interactions between dangerous substance valerate and Anistreplase. (aktuelle-kamera.org)
20201
- 2020. https://nursing.unboundmedicine.com/nursingcentral/view/Davis-Drug-Guide/109358/all/anistreplase. (unboundmedicine.com)
Angiographic1
- Bar and colleagues expressed about the matter: "Angiographic but no clinical improvement after thrombolytic treatment with anistreplase was found in patients with unstable angina with an excess of bleeding complications. (positivehealth.com)
Therapeutic2
- The therapeutic efficacy of Anistreplase can be increased when used in combination with (1,2,6,7-3H)Testosterone. (drugbank.ca)
- The therapeutic efficacy of Anistreplase can be increased when used in combination with 18-methyl-19-nortestosterone. (drugbank.ca)
Patients3
- In a multicenter, double-blind study, patients seen within six hours of the onset of symptoms who had a qualifying 12-lead electrocardiogram were randomly assigned to receive either anistreplase before admission, followed by placebo in the hospital (prehospital group), or placebo before admission, followed by anistreplase in the hospital (hospital group). (nih.gov)
- The study enrolled patients who were treated with anistreplase. (ebscohost.com)
- actavis seeks fda approval for generic Anistreplase to treat pah patients. (sovawinetrail.com)
Stroke2
- severe bleeding or stroke was greater with anistreplase. (thefreedictionary.com)
- Exclusion criteria included history of stroke, active or recent bleeding or major coagulation abnormality, recent trauma or surgery, noncompressible vascular punctures, or previous treatment with streptokinase or anistreplase. (acpjc.org)
Side effects2
- What unwanted side effects would possibly happen because of Anistreplase? (benefits-of.com)
- Although the Pentosan polysulfate sodium in napratec is next included to reduce at the risk calculus of Anistreplase side effects on the gut, these entity types of side effects are mysteries still possible. (aktuelle-kamera.org)
Risk3
- The risk or severity of bleeding can be increased when Anistreplase is combined with (R)-warfarin. (drugbank.ca)
- The risk or severity of bleeding and hemorrhage can be increased when 7,8-Dichloro-1,2,3,4-tetrahydroisoquinoline is combined with Anistreplase. (drugbank.ca)
- The risk or severity of bleeding and hemorrhage can be increased when Aceclofenac is combined with Anistreplase. (drugbank.com)
Form1
- Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. (drugbank.ca)
Case1
- And a case series and literature review, sk and anistreplase induce the opposite direction. (dsaj.org)
Blood1
- Anistreplase is a drug used to stop blood clots. (benefits-of.com)